Background: The Model for End-stage Liver Disease (MELD) 3.0 yields high prognostic performance for patients with end-stage liver disease (ESLD). However, its prognostic performance for patients with alcohol-related liver disease (ARLD) has limited results. The aim of this study was to perform such an evaluation among Chinese patients. Methods: Patients hospitalized with ARLD in one institution between 2015 and 2018 were retrospectively included and followed up for 12 months. The original MELD, MELD-Na, MELD 3.0, and modified Maddrey discriminant function (MDF) scores were calculated for each patient at baseline. Their prognostic performances for 1-year survival were assessed. Time-dependent receiver operating characteristic curves were constructed, and AUCs were calculated for each scoring system. Results: Among the 576 patients included in our analysis, 209 patients had alcoholic hepatitis (AH). By the 1-year follow-up, 14.8% (84/567) of all the patients and 23.4% (49/209) of those with AH had died. Overall, patients who had died had higher MELD, MELD-Na, MELD 3.0, and MDF scores (all p < 0.001) than those who had not. The same was true in the AH subgroup (MELD: p < 0.001, MELD-Na: p < 0.001, MELD 3.0: p = 0.007, MDF: p = 0.017). The AUC of the MELD 3.0 for prediction of 1-year survival among patients with ARLD was 0.682, lower than that of the original MELD (0.728, p < 0.001) and MELD-Na (0.735, p < 0.001). Moreover, in the AH subgroup, the AUC for the prediction of 1-year survival was lower than that in the MELD-Na subgroup (0.634 vs. 0.708, p < 0.001). Conclusions: The MELD 3.0 was not superior to the original MELD or the MELD-Na in predicting the mortality of patients with ARLD.

Background: Currently, there are few studies on the effect of prophylactic anti‐hepatitis B virus (HBV) therapy (AVT) for mother‐to‐child transmission during pregnancy on postpartum hepatitis flare (PHF) and the risk factors for postpartum hepatitis flare in women with chronic hepatitis B infection. Aim: To analyze the effect of AVT on the postpartum hepatitis flare and risk factors related to postpartum hepatitis flare. Methods: This study retrospectively enrolled hepatitis B surface antigen (HBsAg)‐positive and hepatitis B e antigen (HBeAg)‐positive women with HBV DNA ≥ 10⁶ IU/mL. Six hundred fourteen pregnant women were included: 444 in the anti‐HBV therapy group (T‐G) and 170 in the control group (C‐G). To analyze the risk factors, women with alanine aminotransferase (ALT) flare (ALT > 40 U/L) were assigned to the PHF group (PHF‐G, n = 355), and all the others were assigned to a non‐PHF group (NPHF‐G, n = 259). Results: At 6 weeks postpartum, ALT and AST levels were higher, and ALB levels were lower in the C‐G than those in T‐G (P < 0.05). Also, ALT (at baseline, pregnancy 32nd and 36th, intrapartum), AST (at pregnancy 32nd and 36th week, and intrapartum), HBcAb (at baseline, intrapartum), and HBV DNA (at intrapartum) of PHF‐G were significantly higher than those of NPHF‐G (P < 0.05). Multivariate analysis showed that ALT (OR = 1.067, P < 0.001) and HBcAb (OR = 1.213, P ≤ 0.001) in pregnant women were risk factors for PHF. The prophylactic anti‐HBV for the prevention of perinatal HBV transmission (OR = 0.357, P < 0.001) was the protective factor for PHF. Conclusion: Pregnant women with prophylactic anti‐HBV during the third trimester of pregnancy had a lower incidence of postpartum hepatitis flare, especially a lower risk of serious hepatitis flare. ALT and HBcAb in pregnant women were risk factors for PHF. Women infected with HBV should be closely monitored ALT during pregnancy and postpartum.

Background. Few studies explored whether anti-hepatitis B virus (HBV) therapy should be initiated during postpartum hepatitis flare. Aim. This study aimed to analyze the effect of anti-HBV therapy on postpartum hepatitis flare and evaluate the prognosis within 4 years postpartum. Methods. This retrospective study enrolled hepatitis B surface antigen (HBsAg)-positive and hepatitis B e antigen (HBeAg)-positive pregnant women with HBV DNA ≥ 10⁶ IU/mL. A total of 152 pregnant women were included: 103 in the prophylactic anti-HBV therapy group (PT-G) and 49 in the non-prophylactic anti-HBV therapy group (NPT-G). The women with a postpartum flare were assigned to the anti-HBV therapy group (AT-G) and non-anti-HBV therapy group (NAT-G) to analyze the effect of postpartum anti-HBV therapy on hepatitis flare. Virological and biochemical parameters were assessed. Results. Taking postpartum 12 weeks as the cutoff point, the ALT recovered time for postpartum flare women is shorter in AT-G (n = 16, 42.1%) or PT-G (n = 23, 34.8%) than in NAT-G (n = 14, 23.0%; x² = 4.067, ) or NPT-G (n = 4, 11.1%; x² = 5.579, ). Taking postpartum 26 weeks as the cutoff point, the ALT recovered time is shorter in AT-G (n = 35, 57.3%) or PT-G (n = 44, 66.7%) than in NAT-G (n = 32, 84.2%; x² = 7.707, ) or NPT-G (n = 16, 44.4%; x² = 4.749, ). Postpartum flare recovery time was positively correlated with HBV DNA level at delivery [r = 0.223, , 95%CI (0.022～0.41)]. The hepatitis re-flare rates within postpartum 4 years in AT-G (n = 3, 9.68%) is lower than that in NAT-G (n = 24, 45.4%; x² = 14.003, ). The HBeAg, HBsAg, HBV DNA, and ALT level at postpartum 4 years in AT-G were lower than that in NAT-G ( ). Conclusion. Anti-HBV therapy for postpartum hepatitis flare of women with chronic HBV could shorten the ALT recovery time and reduce hepatitis re-flare rates within 4 years of postpartum.

Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) modulates cellular apoptosis, which is involved in the occurrence and development of liver cancer. The mechanisms of apoptosis inhibition by NS5A in liver cancer cells remains unclear. Beclin 1, which functions upstream of autophagosome formation, is upregulated by NS5A. Autophagy, an evolutionarily conserved catabolic process, has a crucial role in tumor initiation and progression. Autophagy was blocked by inhibitors 3‑methyladenine and chloroquine, or via knockdown of Beclin 1. Flow cytometric analysis and western blotting were used to detect apoptosis. It was found that inhibition of autophagy attenuated the NS5A‑mediated apoptosis inhibition of HepG2 cells. Furthermore, it was confirmed that Beclin 1 expression by NS5A was involved in the negative regulation of starvation‑induced liver cancer apoptosis, which was accompanied by reduced p53 and apoptosis regulator Bax expression, as well as decreased caspase‑3/-7 activation. Therefore, inhibition of autophagy may be promising therapeutic strategy in the treatment of HCV‑associated liver cancer.